Recent reports have suggested that increasing the heterogeneity within the parasite's environment, both at an individual and the population level, may help raise the probabilistic barrier of development of resistance in the parasite. The encouraging results following the implementation of a few experimental triple combination therapies like atovaquone-proguanil-artesunate along with the re-emergence of chloroquine sensitive Plasmodium falciparum parasites in the sub-Saharan African nations have re-kindled mankind's hope of curbing anti-malarial drug resistance. The addition of a third drug with traits like a medium half-life and benign safety profile is crucial to achieving SERCAP (single encounter radical cure and preventive therapy), the principle of a triple combination therapy. Simultaneously, the plausible reasons behind the re-emergence of chloroquine sensitive Plasmodium falciparum malaria in the high transmission regions could be the re-expansion of an existing chloroquine susceptible parasite reservoir and a greater predisposition towards the development of polyclonal infections. Another potential reason for this observation could be an impaired deoxyribonucleic acid (DNA) repair mechanisms in the south-east Asian Plasmodium falciparum parasites. These strategies may potentially emerge as the key players in warding off anti-malarial drug resistance in the near future. However, their implementation would be dictated by a host of factors like the epidemiological knowledge, population pharmacokinetics, drug-resistance patterns, cost, availability, and ease of adherence.
A 47-year-old male diagnosed as adenocarcinoma of the lung and received 8 cycles of chemotherapy comprising intravenous administration of cisplatin 125 mg, pemetrexed 850 mg along with zoledronic acid 4 mg. After the completion of the 8 th cycle, the liver enzymes were found to be markedly elevated, evincing zoledronic acid as the cause for hepatotoxicity. The case details were taken from the patient's medical record along with the biochemical test reports and radiographic images. The causal association was confirmed using Naranjo's algorithm and Roussel Uclaf Causality Assessment Method (RUCAM). After the uneventful chemotherapy, patient's liver function tests (LFT) were abnormal. There was an elevation in the aspartate aminotransferase, alanine transaminase, alkaline phosphatase, and direct bilirubin. The causal relationship was established using Naranjo's algorithm (score-6) and RUCAM (score-5), displayed a "probable" and "possible" association. Hartwig's severity scale and Thornton's preventability scale displayed the adverse drug reaction to being moderately severe and not preventable, respectively. The zoledronic acid was stopped and never readministered. The LFTs assumed normal after a span of 2 months. The mechanism underlying hepatotoxicity due to zoledronic acid remains elusive. Zoledronic acid can induce acute phase response mediated by active production of interleukin-6, tumor necrosis factor alpha, and pro-inflammatory cytokines from the T-cells and macrophages. Vigilant monitoring along with timely assessment and management can prevent the occurrence of irreversible liver damage. Henceforth, we would like to report the rare incidence of drug induced hepatic damage due to zoledronic acid. Henceforth, we would like to report the rare incidence of drug induced hepatic damage due to zoledronic acid.
Drugs are known to cause various adverse drug reactions involving major organ systems. Skin-related adverse reactions are very common and range from a simple rash to life-threatening condition like Stevens-Johnson syndrome. Various drugs are known to cause skin reactions which include antiepileptics, analgesics, antibiotics, and proton-pump inhibitors. Nonsteroidal anti-inflammatory drugs causing life-threatening conditions such as Stevens-Johnson syndrome and toxic epidermal necrolysis are very rare and only few case reports are published. Hence, we report a case of Aceclofenac-induced Stevens-Johnson syndrome after single time administration in a tertiary care hospital in India.
PPIs are not entirely free of adverse effects, as assumed by several practitioners. A vigilant eye has to be maintained on the patient's renal profile so as to avoid any untoward decline in renal function, as evidenced in the current study.
Background: The peptic ulcers can be developed inside the inner lining of the stomach (gastric ulcer) or the small intestine (duodenal ulcer). Around 10% population of the world is suffering from the peptic ulcer disease. From the ancient times there is a reference about herbal extracts like Sesame indicum for the treatment of various diseases. The aim of the study is Evaluation of the anti-peptic ulcer activity of the seed extract of sesame (Sesamum indicum) in stress induced peptic ulcers in rats.Methods: The study was carried out by stress-induced ulcer model in wistar rats. The antiulcer activity of S. indicum (0.5, 1mg/kg p.o. for 7 days) was compared with standard drugs (pantoprazole). The studied parameters were mucin content, gastric volume, pH, total acidity, free acidity, ulcer index, size and number.Results: The low and high dose of S. indicum extract significantly reduced gastric mucosal lesion, mucin content, volume of gastric juice, gastric pH, free and total acidity when compared to positive control group. The high dose of S. indicum extract showed comparable results in parameters like effect on mucin content, gastric volume, pH, free acidity and total acidity with standard group. The statistical significant changes noted only in ulcer size, number and index.Conclusions: Although the high dose S. indicum (1mg/kg) group showed significant gastric protection against ulcer induced by cold restraint method. However, no clear inference can be drawn at this stage and hence there is a need for further extensive research.
When an infected patient suffers from thrombocytosis, it is very difficult to identify beta-lactam antibiotic-induced cases of the disease and separate those from the possibility that thrombocytosis is an acute-phase reaction in the infected patient. We present 3 cases who were treated with Augmentin for various indications and developed thrombocytosis during the treatment course. The Naranjo probability scale indicates Augmentin as the possible cause of the thrombocytosis in all our patients.
Cutaneous adverse drug reactions are very common in a hospital setting while treating patients. Drug-induced vasculitis is a very common form of vasculitis affecting all age groups, and many drugs have been implicated in causing vasculitis. Clopidogrel is an antiplatelet drug used in the management as well as prevention of coronary artery disease. It is known to cause various side effects ranging from bleeding, gastrointestinal disturbances, to skin rashes. Leukocytoclastic vasculitis is a form of hypersensitivity vasculitis and is very rarely seen with clopidogrel. Hence, we report a case of clopidogrel-induced leukocytoclastic vasculitis in an old male patient after coronary stenting.
Melioidosis is a fatal disease, most prevalent in South-East Asia, Northern Australia, and the Indian subcontinent is caused by Gram-negative saprophyte Burkholderia pseudomallei. Septic arthritis due to melioidosis is very rare and should be a differential diagnosis in patient presenting with septic arthritis in endemic areas. It results in severe morbidity. Hence, we report a case of septic arthritis of left knee and hip in a young patient who later developed pleural effusion caused by B. pseudomallei.
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